WOFAPS 2025 8th World Congress of Pediatric Surgery

Ting Chen ¹, Kai Bin Liew ², Mei Hua Tan ³

¹ Faculty of Pharmacy, University of Cyberjaya, Persiaran Bestari, 63000 Cyberjaya, Selangor, Malaysia; Department of Pediatric Orthopaedic, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
² Faculty of Pharmacy, University of Cyberjaya, Persiaran Bestari, 63000 Cyberjaya, Selangor, Malaysia
³ School of Biotechnology, Mila University, No. 1, Persiaran MIU, 71800 Nilai, Negeri Sembilan, Malaysia

Objective: To explore the mechanism of FOXO1 on the regultion of developmental dysplasia of the hip (DDH). Methods:(1)Clinical experiment: 40 patients with DDH were enrolled and the general clinical data were collected. Assess hip joint function of the patients were evaluated using McKay Hip Score. FOXO1 concentrations in the serum were detected by ELISA assays. The relationship between FOXO1 concentration and DDH severity was investigated by statistical analysis. (2)Animal experiments: DDH rat model was builded, then divided into control group and model group. Femoral head morphological index was measured. The cartilage degradation was evaluated by FOXO1 immunohistochemical staining, HE staining and Mankin scoring. (3)Cell experiments: The hip joint chondrocyte was isolated from control and model group rat and then transfected with siFOXO1 plasmid. Cell proliferation was detected by WST1 assay. Cell apoptosis was detected by flow cytometry. The expressions of FOXO1, β-catenin and Bim were detected by qRT-PCR and western blot assay. Results: FOXO1 level in the serum of DHH patients correlated negative correlation with the DHH severity. Femoral head morphological index of model group was higher than that of control group. HE staining results showed significant pathological changes in the hip joints of the model group animals. Immunohistochemistry results indicated decreased FOXO1 expression levels in the hip joint tissues of the model group. The cell proliferation index in model group was lower than that of control group, and the cell apoptosis was induced in model group. Compared with control group, the β-catenin and Bim expression level were upregulated. The apoptosis was inhibited, the proliferation, β-catenin and Bim expressions were increased after siFOXO1 plasmid transfected in model group. Conclusions: FOXO1 could regulated chondrocytes apoptosis via Wnt/β-catenin signal pathway, and then improve clinical symptoms of DHH